The disclosure herein relates to methods and devices for modifying atrioventricular delays based on activation times within cardiac tissue to, e.g., maintain effective pacing therapy.
In the normal human heart, the sinus node, generally located near the junction of the superior vena cava and the right atrium, constitutes the primary natural pacemaker initiating rhythmic electrical excitation of the heart chambers. The cardiac impulse arising from the sinus node is transmitted to the two atrial chambers causing a depolarization and the resulting atrial chamber contractions. The excitation pulse is further transmitted to and through the ventricles via the atrioventricular (AV) node and a ventricular conduction system causing a depolarization and the resulting ventricular chamber contractions.
Disruption of this natural pacemaking and conduction system as a result of aging or disease can be treated by artificial cardiac pacing. For example, one or more heart chambers may be electrically paced depending on the location and severity of the conduction disorder. In addition, cardiac pacing for ventricular dyschrony, often referred to as cardiac resynchronization therapy (CRT), may include pacing one or both ventricles before normal conduction through the AV node depolarizes the ventricles.
Implantable medical devices (IMDs) are capable of utilizing pacing therapies, such as CRT, to maintain hemodynamic benefits to patients. Pacing therapy may be delivered from an implantable generator, through a lead, and into the patient's heart. Basic programmable pacing parameters include atrioventricular delay (AV delay), left ventricle to right ventricle delay (VV delay), pacing amplitude, pacing rate, pulse duration, and pacing pathway or vector (e.g., bipolar such as a lead tip electrode to a lead ring electrode, etc. or unipolar such as a lead tip electrode to IMD casing, or housing), which all may be configured to ensure effective therapy to the patient.
For some patients suffering from heart failure and intraventricular conduction delays due to, e.g., left bundle branch block, right bundle branch block, the delivery of CRT can occur due to a single ventricular pacing stimulus by pre-exciting the ventricle with conduction delay. Such a stimulus must be properly timed relative to intrinsic depolarization of the other, non-delayed ventricle. This phenomenon may be referred to herein as “fusion pacing” since ventricular activation from a pacing stimulus fuses or merges with ventricular activation from intrinsic conduction. When the ventricular pacing stimulus is properly timed a desired ventricular resynchronization results with a minimum of pacing energy, thereby extending the operating life of an implantable pulse generator (e.g., an implantable cardioverter-defibrillator, pacemaker, and the like). Moreover, in some cases a more effective or physiologic form of CRT delivery can be achieved since the system and methods herein utilize a portion of intrinsic activation, which can be superior to an entirely evoked (e.g., paced) form of CRT. Fusion pacing may also be referred to herein as left ventricle-only pacing or right ventricle-only pacing.
One method of fusion pacing, or left ventricle-only pacing, includes pacing the left ventricle at an appropriate time to achieve fusion of a paced wavefront with an intrinsic depolarization of the right ventricle. One method of fusion pacing, or right ventricle-only pacing, includes pacing the right ventricle at an appropriate time to achieve fusion of a paced wavefront with an intrinsic depolarization of the left ventricle. Such a CRT method may reduce device power output relative to biventricular pacing and may improve hemodynamics, especially at lower heart rates.
One specific parameter that may be used by an IMD to deliver cardiac therapy (e.g., CRT such as left ventricular fusion pacing) is an atrioventricular delay (AV delay), which may generally be described as a programmable value representing a time period between atrial electrical activity, whether intrinsic (e.g., natural) or paced, and the delivery of ventricular pacing. The optimal value of the AV delay has generally been defined as a delay that produces the maximum stroke volume for a fixed heart rate or the maximum cardiac output for a sinus node driven heart rate.
To optimize or adjust the AV delay, a cardiac therapy device such as an IMD may measure a patient's intrinsic AV conduction time. A patient's intrinsic AV conduction time is the time between an intrinsic atrial event (e.g., depolarization of the right atrium) and an intrinsic ventricular event (e.g., depolarization of the right ventricle). As used herein, an “intrinsic” event or conduction is one that occurs or is conducted naturally (e.g., an intrinsic ventricular event is an event triggered by electrical activity transmitted across the AV node of the heart from the atria to the ventricles, etc.). A cardiac therapy device may periodically measure a patient's intrinsic AV conduction time, or interval, and adjust the AV delay in response to the measured intrinsic AV conduction time, e.g., to optimize cardiac functionality.
For example, a CRT algorithm (e.g., performed by an IMD) may measure a patients intrinsic AV conduction time once every minute by forcing delays used for ventricular pacing (e.g., paced AV delay, sensed AV delay, etc.) to long values (e.g., 300 milliseconds (ms), 350 ms, etc.). Conventionally, the intrinsic AV conduction time measurement has been performed periodically (e.g., every 60 seconds) so that the CRT algorithm can adapt to changes in the patient's intrinsic AV conduction time.
In other words, CRT algorithms may temporarily suspend, or interrupt, pacing therapy for one or more heartbeats to measure a patient's intrinsic AV conduction time for use in modifying or adjusting (e.g., optimizing) one or more pacing parameters such as AV delay.